The human immune response is regulated by a highly complex and intricate network of control elements. Prominent among these regulatory components are the anti-inflammatory cytokines and specific cytokine inhibitors. Under physiologic conditions, these cytokine inhibitors serve as immunomodulatory elements that limit the potentially injurious effects of sustained or excess inflammatory reactions. It has been demonstrated that proinflammation has an association with pathophysiology and is connected with various clinical disease manifestations (Kalogeropoulos et al. J. Am. Coll. Cardiol. 2010, 55, 2129). Several dominant proinflammatory cytokines, such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), are involved in the pathogenesis of cardiovascular and nuerodegenerative diseases and cancers through a series of cytokine signaling pathways. Over-expression of cytokines in both mRNA and protein levels is responsible for a number of pathological conditions like ulcerative colitis, diabetes, atherosclerosis, stroke, Alzheimer's disease, and cancer (Ait-Oufella et al. Arterioscler. Thromb. Vasc. Biol. 2011, 31, 969; Grivennikov and Karin, Ann. Rheum. Dis. 2011, 70, i104). Several cytokines, such as TNF-α, IL-6, and IL-1β, have received a considerable amount of attention as molecular targets for treatment of diseases mentioned above. The inhibition of cytokines, particularly TNF-α, has been successful in several clinical trials for treatment of cancer and rheumatoid arthritis. In addition, it is believed that mast cells, neutrophils, and macrophages which secrete inflammatory factors are the important players in inflammatory disorders. Inhibition of release of cytokines in activated macrophages has become a focus of current drug discovery and development and an important method for evaluating the bioactivity of drugs (Jeremy S. D. Sem. Nephrol. 2010, 30, 234).